Jennifer A. Philips, M.D., Ph.D.

Assistant Professor
Internal Medicine
Infectious Diseases
Molecular Microbiology

Molecular Microbiology and Microbial Pathogenesis Program
Immunology Program
Molecular Cell Biology Program

  • 314-747-8058

  • 8051

  • 7th Floor McDonnell Pediatrics Research Building



  • tuberculosis, host-pathogen interactions, innate immunity, autophagy, phagosome maturation, antigen presentation, macrophage, ESCRT

  • Immune Evasion by Mycobacterium tuberculosis

Research Abstract:

Mycobacterium tuberculosis (Mtb) causes tuberculosis (TB), one of the world’s most deadly infections. Mtb disrupts anti-microbial pathways of macrophages, cells that normally kill bacteria. Mtb establishes persistent infection despite inducing robust antigen specific T cell responses. How Mtb undermines these host immune functions is the focus of our work. We are identifying and characterizing host-pathogen interactions that provide mechanistic insight into how Mtb alters cellular trafficking, lipid handing, antigen presentation, and cytokine responses of macrophages and dendritic cells. In studying the molecular mechanisms by which Mtb sabotages cellular functions, we hope to better understand host immunity and bacterial pathogenesis

Selected Publications:

Tinaztepe, E., Wei, J-R., Raynowska, J., Thompson, V., and Philips, J.A. (2016) The role of metal-dependent regulation of ESX-3 secretion on the intracellular survival of Mycobacterium tuberculosis, Infect Immun, May 31, pii: IAI00197-16 [Epub ahead of print]; PMID:27245412.

Ouimet M, Ediriweera H, Ramkhelawon B, Hennessy E, Sakowski E, Koster S, Portal-Celhay C, Ray T, Sheedy F, Karunakaran D, Singaravelu R, Van Solingen C, Liao X, Pezacki JP, Tabas I, Marcel Y, Rayner KJ, Philips JA,* Moore KJ.* (2016) Mycobacterium tuberculosis induces the miR-33 locus to inhibit autophagy and reprogram host lipid metabolism, Nat Immunol 17, 677-686. PMCID: PMC4873392.

Tufariello, J.M., Chapman, J.R., Kerantzas, C.A., Wong, K.W., Vilcheze, C., Jones, C.M., Tinaztepe, E., Thompson, V., Fenyo, D., Niederweis, M., Ueberheide, B., Philips, J.A.*, and Jacobs, W.R. Jr*. (2016) Separable roles for Mycobacterium tuberculosis ESX-3 effectors in iron acquisition and virulence. Proc Natl Acad Sci USA 113, E348-E357. PMCID: PMC4725510.

Sakowski, E., Koster, S., Portal Celhay, C., Park, H.S., Shresthra, E., Hetzenecker, S. E., Maurer, K., Cadwell, K., and Philips, J.A. 2015. Ubiquilin-1 Promotes IFN-gamma-Induced Xenophagy of Mycobacterium tuberculosis, PLOS Pathogens, 11:e1005076.

Vaeth, M., Zee, I., Concepcion, A.R., Maus, M., Shaw, P., Portal-Celhay, C., Zahra, A., Kozhaya, L., Weidinger, C., Philips, J., Unutmaz, D., and Feske, S. 2015. Ca2+ Signaling but not Store-Operated Ca2+ Entry Is Required for the Function of Macrophages and Dendritic Cells. J. Immunol, 195:1202-1217.

Siegrist, M.S., Steigedal, M., Ahmad, R., Dragset, M.S., Mehra, A., Philips, J.A., Carr, S.A., and E.J. Rubin. 2014. Mycobacterium Esx-3 Requires Multiple Components for Iron Acquisition, Mbio. 5: e01073-14; PMID 24803520

Mehra, A., Zahra, A., Thompson, V., Sirisaengtaksin, N., Wells, A., Porto, M., Penberthy, K., Kubota, Y., Dricot, A., Rogan, D., Vidal, M., Hill, D.E., Bean, A. J. and Philips, J.A. 2013. Mycobacterium tuberculosis Type VII secreted effector EsxH targets host ESCRT to impair trafficking, PLOS Pathogens, 9:e1003734; PMID 24204276.

Philips, J.A. and Ernst, J. D. 2012. Tuberculosis and Immunity, Annu. Rev. Pathol, 7: 353-384. PMID: 22054143

Philips, J.A., Wang, H., Rubin, E.J., and Perrimon, N. 2008. ESCRT Factors Restrict Mycobacterial Growth, Proc. Natl. Acad. Sci. 105: 3070-3075; PMID 18287038.

Philips, J.A., Rubin, E.J., and Perrimon, N. 2005. Drosophila RNAi Screen Reveals CD36 Family Member Required for Mycobacterial Infection. Science 309, 1251-1253; PMID 16020694.

Agaisse, H., Burrack, L. S., Philips, J.A., Rubin, E.J., Perrimon, N., and Higgins, D.E. 2005. Genome-wide RNAi Screen for Host Factors Required for Intracellular Bacterial Infection. Science 309, 1248-1251; PMID 16020693.

*Co-corresponding, equal contribution.

Last Updated: 9/6/2016 9:32:12 AM

Back To Top

Follow us: